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Standard Gene Set NameBAE_NEP1_30MIN_DN
SpeciesArabidopsis thaliana
Brief DescriptionDown-regulated by 30 min treatment with 10 mg/ml Nep1 (Table S1 PubmedID:16698904)
Full Description/AbstractTreatment of Arabidopsis thaliana with a necrosis- and ethylene-inducing peptide (Nep1) from Fusarium oxysporum, inhibited both root and cotyledon growth, and triggered cell death, thereby generating necrotic spots. Nep1-like proteins are produced by divergent microbes many of which are plant pathogens. Nep1 in the plant was localized to the cell wall and cytosol based on immunolocalization results. The ratio of chlorophyll a fluorescence (F685nm/F730nm) significantly decreased after 75 min treatment with Nep1 in comparison to the control. This suggested that a short-term compensation of photosynthesis occurred in response to localized damage to cells. The concentrations of most water-soluble metabolites analyzed were reduced in Arabidopsis seedlings after 6 h of Nep1 treatment, indicating that the integrity of cellular membranes had failed. Microarray results showed that short-term treatment with Nep1 altered expression of numerous genes encoding proteins putatively localized to organelles, especially the chloroplast and mitochondria. Short-term treatment with Nep1 induced NA classes of genes involved in reactive oxygen species production, signal transduction, ethylene biosynthesis, membrane modification, apoptosis, and stress. Quantitative PCR was used to confirm the induction of genes localized in the chloroplast, mitochondria and plasma membrane, and genes responsive to calcium/calmodulin complexes, ethylene, jasmonate, ethylene biosynthesis, WRKY, and cell death. The majority of Nep1 induced genes have been associated with general stress responses, but have not been critically linked to resistance to plant disease. These results are consistent with Nep1 facilitating cell death as a component of diseases caused by necrotrophic plant pathogens
External Pathway ID/Pubmed ID16698904
SourceLiterature
Contributor/AuthorLiming Lai and Xijin Ge
Organization of contributerSouth Dakota State University
External URLhttp://www.plantphysiol.org/cgi/rapidpdf/pp.106.076869v1